Seeing life differently.

I was really excited tonight when my friends at the Asthma Society of Canada shared an article entitled Six research developments in asthma via Healio. I think it’s important for patients to know what’s going on in research, and hopefully, the more people see what’s going on, the more people feel the desire to volunteer as participants in asthma research studies (like the Severe Asthma Research Program) or clinical trials that they are eligible to participate in.

The disappointing reality, though, is these “research developments” really contain little new knowledge. Some of these facts have been circulating around for a few years if you’ve been paying attention—and others, well, while I have a larger knowledge base on asthma than the average person with asthma [and, admittedly, some medical professionals], I am not a medical professional or researcher, and . . . I could have concluded the same thing, just less scientifically. Some others, well, point six for example? I knew from the title I wouldn’t understand, so I am admitting defeat on that right now.

Note that while I’ve linked a lot of studies here, I tried to keep my explanations basic [because, that’s the only way I actually understand].

2. “E-cigarettes may worsen asthma, respiratory disease among youth.” You’re joking, right? Inhaling a nicotine based chemical vapour might cause asthma symptoms? “Among youth” is also the key phrase here—for only the reason that it should be “among people”. I react to chemicals–from perfume or cologne, to body lotions, to Lysol—with exposure, never mind with purposefully inhaling stuff.

3. “Asthma relapse more likely after use of short-acting beta-2 agonists.” A beta-2 agonist is just the fancy term for a bronchodilator [a medicine that widens narrowed airways]; short acting ones [SABAs] are the common rescue inhalers that work within a few minutes and last for 4-6 hours. In more detail, the study reports that if SABAs are used prior to going to the hospital, relapse—or what some hardcore asthmatics would call rebounding—is more likely to occur. I actually need to quote this one out here because it’s so ridiculous:

Children who took short-acting beta-2 agonists within 6 hours before hospital admission and the presence of retractions on physical examinations increased their risk for relapse after the treatment for asthma exacerbations, according to data.

Obviously the best line is “according to data” (which you can find here—the full text, however, costs $30 despite that I am on my university’s database network—so, I, possibly like the authors of this article, won’t be digging any deeper). Given the line about SABA use, clearly this is useless data: if a person has an inhaler accessible, why would they not be using it? That’s what it’s for.
We get a bit smarter when we note the “presence of retractions” (decreased ability of the lungs to move air causes the muscles attached to the ribs—allowing the space around the lungs to become larger or smaller [more here on respiratory mechanics]–start working overtime, pulling inward to compensate for respiratory distress. Like I said, I’m not a scientist… but, I’m pretty sure recovering respiratory distress pretty automatically qualifies you to rebound. That, or tapering from the high dose steroids they suggest as a positive measure in preventing relapses. The final point, providing a written plan, is clearly a good one, and if anything is being done to be useful, probably more psychosocial research should fill the gap for what medicine is having trouble providing.

4. “Antibiotic use in first year of life associated with asthma by age 3.” I was diagnosed with asthma in April 2008. Like any sixteen-year-old, I read Wikipedia. Know what Wikipedia told me six years ago? That I had a higher chance of developing asthma because I was a) given antibiotics early in life, b) born premature, c) born by caesarean section. Wikipedia revealed this to me in 2008. Nope, I wasn’t diagnosed when I was three [or seven] but obviously, this is hardly new. If you’re already tired of my links and didn’t click through, that first abstract above [Droste et al.] is from 2000.

5. “Vitamin D3 treatment did not significantly affect asthma patients with low vitamin D levels.” This one is a newer area of exploration [but certainly not as new as 2014…], and to its credit [in my books, at least], its potentially tangible to patients. Initially, studies suggested that vitamin D might alter immune response to some degree (2007 article here for those smarter than me). While the article cited by Healio bases its notation on a single study, a meta-analysis and systematic review of the literature (Zhang, Gong & Liu, 2014) note that among 10 studies, while asthmatics were more likely to have vitamin D deficiency than control subjects [non-asthmatics], their vitamin D levels didn’t alter their asthma symptoms. Thus, what I take from this, is I can continue to avoid the outdoors as much as I want. [Kidding :).]

6. Hardcore science. The sixth point is far too complicated for me to even begin to discuss, so you smart people who understood that 2007 article up there on vitamin D, can please feel welcome to report back to us about elevated urinary diclorophenol and asthma morbidity. Because, like I said, not a scientist, and that is clearly not applicable to my life.

Research is research, and I’m happy it’s being done—but, I am here now. The above findings are not affecting my daily reality, and I’m not sure they’re getting us any closer to doing so.

While a few legitimately new asthma drugs have hit the market recently (primarily biologics like Xolair) I—and most asthma patients—are either using medications developed 30 or 40 years ago, or variations of medications developed in that timespan The medicine every asthmatic should have access to, most commonly known as Ventolin (salbutamol/albuterol in the US), was developed in 1968. Yet, here I am, forty-sixyears later, still taking this same bronchodilator medication because the alternatives aren’t available, and even if they were, aren’t really proven to be any more effective (Xopenex, to name one, is not available in Canada—levosalbutamol/levalbuterol is alleged to have fewer cardiac side effects, but… at a much higher price, thus, its much more rarely prescribed). Next up as the most-common asthma medicine type? Inhaled steroids—initially developed in, you guessed it, the 1960s. We’ve had a few more advances in terms of, say, long-acting bronchodilators, but salmeterol (Advair/Seretide/Serevent)—and less dramatically, formoterol (Symbicort/Dulera/Zenhale/Foradil) carry a black box warning of increased risk of asthma related death. Know what else causes asthma related death? Asthma.

Knowing that my risk of lung cancer is reduced is great, but maybe that’s not so much a “protective effect” but a biased finding as asthmatics [especially lesser-controlled ones] are often asked if we smoke by medical people—thus increasing our chances of smoking cessation intervention if perhaps we do smoke.

It doesn’t change that right now, today, I’ve used four different inhalers to stay feeling decent. Nope, not normal, not magically controlled… but decent. It doesn’t change that I’ve tried most available asthma medications and while the ones I am on now are the best fit for me so far, I still don’t know when that next thing that could be my “wonder drug” could come along—or if it ever will. We still barely know what causes this disease—other than it’s probably a combination of environment and genetics—so how can we even consider having the ability to find an actual cure for this disease? I honestly don’t think we can—and, here’s where my optimism severely drops: I very much doubt we will in my lifetime.

I just hope that next time I see a top six in research developments, that instead of telling me nothing that changes my daily life, that maybe we know what causes this disease and that it’s become preventable. That maybe they’ve developed an accessible system to phenotype asthma (nod to researchers like Dr. Sally Wenzel working on this right now!) and from that, can throw—hopefully new, and not just newly reformulated—medicine at me that will be guaranteed to work.

And even, most simply, that the psychosocial, emotional, and developmental aspects of the disease are addressed and that this knowledge is applied everywhere possible: to promote better patient and community education that’s developmentally and culturally appropriate for every community; to provide better patient-to-patient support—in a way that’s implementable and sustainable; and to ensure people understand their asthma and understand how to self-advocate.

The science is cool, or at least on its way to being cool—the science will eventually be awesome—but even when new ways to manage—or even cure—asthma arise, I know that if I’m still around that I probably won’t be able to trust the process fully if I don’t have a community of people sharing my story, sharing in similar circumstances, alongside me in whatever that undiscovered path might look like to be adjusting alongside me, too.

Great post. I identify with a lot of what you’ve written (except that I didn’t read the articles). I am overall pretty satisfied with my asthma control regimen. Of course its not perfect, but its pretty good. I take it in stride and life goes on. I hardly ever think about a cure since I’m pretty sure its unlikely I’ll ever see one.

Meh. I’m not really optimistic about research either. As you said, there has been very little change. And overall, I am happy where I am (or at least used to it) and pretty stable. Given that, I am uninterested in volunteering my lungs/body for research. My asthma has been more controlled now and in the past few years than it was ever in my life. I don’t want to switch up my meds/treatment and mess with that.

Actually, recent study on the antibiotic link suggests asthma causation might have nothing to do with antibiotics at all – that antibiotic use <3YO correlates with asthma because people with asthma tend to be genetically more vulnerable to viral infections, which in turn makes you more likely to get serious viral infections (RSV, etc), which are often treated with antibiotics until bacterial infection is ruled out. It also makes you more likely to get secondary bacterial infections, which are treated with antibiotics. Both of the previous more likely to get lung damage which makes you more likely to get asthma. When you combine that with a genetic predisposition toward atopy, bam asthma. Which would explain why they're strongly correlated, without a causative effect being necessary.

Right, but that [to me] still doesn’t add up if the infections/antibiotic use precede the asthma, which I think was the point, no? I don’t disagree that they can be correlated but not causative, but in certain situations, if research is suggesting a potentially causative link [which, like most things, there are always exceptions to], the link could potentially be more direct.

Additionally, I didn’t immediately correlate antibiotic use with respiratory infections (as in being used for respiratory infections) — that’s just simply because of my own history that I didn’t make that correlation [I had massive doses of antibiotics early in life for a systemic staph infection(/sepsis), so not directly affecting my lungs]. So certainly that’s a good point, too.

For whatever it’s worth, I tried Xopenex samples from my doctor several years ago and found the effects uneven and far inferior to albuterol, but my asthma is severe and atypical (I was diagnosed in 1983 at age 18).

Hi Lorena,
Apologies for the delay–I just realized I wasn’t getting e-mail alerts for comments!
Sorry to hear your asthma is so bad. In terms of the Xopenex discussion, it’s really just because it’s unavailable in Canada that it sucks, you know? I could try it and have the same experience as you, but it’s the fact that I can’t even ACCESS it that sucks. Even if they don’t work, it’s nice to have options!